Plasma triglycerides are transported in the plasma from the gut as chylomicrons and from the liver as very low density lipoproteins (VLDL). These triglyceride-rich lipoproteins are degraded in extra-hepatic tissues (primarily muscles and adipose tissue) by an enzyme known as lipoprotein lipase. Intravenous injection of heparin releases lipoprotein lipase into the plasma. A second enzyme from the liver (hepatic tryglyceride lipase or H-TGL) also appears in plasma immediately after heparin is injected. The function of this latter enzyme is not clearly understood. Techniques have been developed for the isolation of these two enzymes from postheparin plasma and from tissues. Current evidence indicates that the hepatic triglyceride lipase and lipoprotein lipase for adipose tissue are very similar in their molecular structure. However, these enzymes differ markedly in a variety of characteristics that relate to their activity. This proposal outlines a series of experiments to define the structural and functional differences between these two enzymes in human and swine. The initial series of experiments proposes to investigate the oligosaccharide components of the two enzymes since the polypeptide chain appears to be identical. The oligosaccharides are to be isolated and their exact sugar composition and the nature of their linkage to the protein defined. The two enzymes are immunochemically distinct and, therefore, antisera can be utilized to determine differences in structure. The antisera will also be utilized in the development of a radioimmunoassay for each form of the enzyme in both human and swine. This radioimmunoassay will be utilized to determine the presence of inactive as well as active enzyme protein for comparative studies with activity. These tools will allow the study of the process of enzyme synthesis, storage and secretion from the cell utilizing swine tissue. Metabolic ward studies in humans with hyperlipoproteinemia and in normal controls will be undertaken to determine regulation of low enzyme activity and mass in the plasma and in adipose tissue biopsies. With these tools, better definition of the factors regulating the enzyme activity under normal and disordered metabolic states can be better defined. Finally, subjects with Type I hyperlipoproteinemia will be studied. These individuals have little or no lipoprotein lipase detectable by assays for activity. Thes (Text Truncated - Exceeds Capacity)